Saint Vincent Hospital

AIMS:Catheter-based therapies for pulmonary embolism (PE), including endovascular mechanical thrombectomy (MT) and catheter-directed thrombolysis (CDT), are increasingly being used in clinical practice. However, real-world comparative data between these two modalities are scarce. We aimed to evaluate and compare the outcomes of MT and CDT in patients with PE. METHODS AND RESULTS:This retrospective cohort study utilized the 2021 National Readmission Database (NRD) to identify adults with a primary diagnosis of PE who underwent either MT or CDT. The primary outcome was in-hospital mortality, while secondary outcomes included major bleeding, cardiac arrest, vascular complications, and post-discharge readmissions. Propensity-score matching was applied, followed by logistic and Cox-proportional hazard regression analyses. Subgroup analyses were conducted based on hospital procedural volume. After propensity-score matching, 7376 patients who underwent MT and 7355 who underwent CDT were included. MT was associated with higher odds of in-hospital mortality (4.4% vs. 3.4%; OR: 1.31, 95% CI: 1.01-1.68; P = 0.04) and major bleeding (6.3% vs. 3.6%; OR: 1.79, 95% CI: 1.39-2.32; P < 0.001) compared with CDT. No significant differences were observed in post-discharge mortality, although all-cause readmissions were higher in the MT group. Higher hospital procedural volumes were associated with lower in-hospital mortality and lower major bleeding rates in both MT and CDT. CONCLUSION:Endovascular CDT was associated with lower in-hospital mortality and major bleeding compared to MT in PE. As hospital procedural volume increased, both these outcomes improved, while difference in outcomes between MT and CDT reduced.

The cardiovascular diseases (CVDs) are a primary global health concern with significant mortality and morbidity. Recent findings suggest that gut microbiota, through its complex interactions with host metabolism, immune response, and inflammation, plays a crucial role in the pathogenesis and progression of CVD. The mechanisms linking gut dysbiosis with cardiovascular risk factors such as hypertension, atherosclerosis, and metabolic syndrome offer a novel perspective on heart health. Excitingly, interventions targeting the microbiome, such as dietary adjustments, probiotics, and prebiotics, hold promise in reducing CVD risks. Adopting personalized approaches to microbiome therapy, tailored to individuals’ unique microbial profiles, could usher in more effective treatments for CVD. As research continues to unveil the intricate role of the gut microbiome, the future of CVD treatment and prevention appears poised for significant transformation. Therefore, this burgeoning field promises to bring about a paradigm shift in cardiovascular health management, with a strong emphasis on personalized, microbiome-based therapeutic strategies, and preventive measures through diet and lifestyle modifications. This review aims to emphasize the potential of integrating the gut microbial insights into clinical practice and how it can be exploited to revolutionize the prevention and management of CVD in future.

Metabolic dysfunction-associated fatty liver disease (MAFLD) is a growing global health concern which is driven by the increasing prevalence of diabetes and obesity. MAFLD is characterized by excessive fat accumulation in the liver, which encompasses a range of conditions, from simple hepatic steatosis to more severe forms. This condition is associated with various complications, including chronic kidney disease (CKD), Cardiovascular Disease (CVD), liver cirrhosis, and even malignancy. Recent research has highlighted a potential connection between gut dysbiosis and MAFLD, particularly in relation to CKD. This has underscored the significance of the gut-liver-kidney axis in understanding MAFLD's pathogenesis. Inflammation triggered by MAFLD increases the risk of CVD through multiple mechanisms linked to metabolic dysfunction. These mechanisms include heightened oxidative stress, systemic and hepatic insulin resistance, low-grade inflammation, and endothelial dysfunction. Hepatic steatosis and metabolic dysfunction are major diagnostic criteria for MAFLD, often coexisting with other liver ailments. This prospective review emphasizes the intricate associations between MAFLD, cardiovascular complications, renal issues, and hepatic diseases. Understanding the underlying pathophysiological pathways is crucial in comprehending the increased risk of CKD, CVD, and other hepatic complications in individuals with MAFLD.

This review was written to inform practicing clinical rheumatologists about recent advances in artificial intelligence (AI) based research in rheumatoid arthritis (RA), using accessible and practical language. We highlight developments from 2023 to early 2025 across diagnostic imaging, treatment prediction, drug discovery, and patient-facing tools. Given the increasing clinical interest in AI and its potential to augment care delivery, this article aims to bridge the gap between technical innovation and real-world rheumatology practice. Several AI models have demonstrated high accuracy in early RA detection using imaging modalities such as thermal imaging and nuclear scans. Predictive models for treatment response have leveraged routinely collected electronic health record (EHR) data, moving closer to practical application in clinical workflows. Patient-facing tools like mobile symptom checkers and large language models (LLMs) such as ChatGPT show promise in enhancing education and engagement, although accuracy and safety remain variable. AI has also shown utility in identifying novel biomarkers and accelerating drug discovery. Despite these advances, as of early 2025, no AI-based tools have received FDA approval for use in rheumatology, in contrast to other specialties. Artificial intelligence holds tremendous promise to enhance clinical care in RA—from early diagnosis to personalized therapy. However, clinical adoption remains limited due to regulatory, technical, and implementation challenges. A streamlined regulatory framework and closer collaboration between clinicians, researchers, and industry partners are urgently needed. With thoughtful integration, AI can serve as a valuable adjunct in addressing clinical complexity and workforce shortages in rheumatology.

VEXAS syndrome (Vacuoles, E1 enzyme, X-linked, Autoinflammatory, Somatic) is a recently identified autoinflammatory disorder caused by somatic UBA1 mutations. It presents with intractable systemic inflammation and hematologic abnormalities. Diagnostic delay and limited therapeutic consensus pose challenges in clinical practice. To illustrate the phenotypic heterogeneity and therapeutic response in two patients with genetically confirmed VEXAS syndrome, and to conduct a targeted narrative review of the literature focused on treatment outcomes. Two adult male patients presenting with multisystem inflammatory features and cytopenias were diagnosed with VEXAS syndrome via detection of somatic UBA1 mutations on next-generation sequencing. To contextualize these cases, we performed a narrative literature review using PubMed, Scopus, Web of Science and, Directory of Open Access Journals (DOAJ) for studies published up to October 2024. Search terms included “Autoinflammatory Diseases,” “Mutation, Somatic,” “Ubiquitin-Activating Enzymes,” “Glucocorticoids,” “Biologic Therapy,” and “Stem Cell Transplantation.” Only peer-reviewed, English-language studies involving adult human patients with clinically characterized VEXAS syndrome were included. Pediatric cases and reports limited to genomic analysis without clinical correlation were excluded. Both patients exhibited classic features of VEXAS, including multisystem inflammation and cytopenias. Genetic sequencing confirmed UBA1 mutations. Treatment with corticosteroids combined with biologic agents such as tocilizumab in one patient and canakinumab in the other achieved clinical stabilization while allowing for reduction of corticosteroid doses. Literature review indicates that while glucocorticoids remain first-line therapy, IL-1 and IL-6 inhibitors demonstrate promising steroid-sparing efficacy in selected patients. Data on long-term outcomes and standardization of care remain limited. These cases reflect the diagnostic and therapeutic complexities of VEXAS syndrome. A high index of suspicion, followed by genetic testing, is essential for timely diagnosis. Biologic therapies targeting IL-1 and IL-6 pathways may offer effective steroid-sparing options in refractory cases. Further prospective studies are needed to define optimal treatment strategies.